Background Research

Dictyostelium discoideum is a single-celled amoeba that has shown great promise in the modeling of cancer cells because of their various similar behaviors. One behavior that is greatly studied is the ability of D. discoideum cells to aggregate, which can be used to model the cell-to-cell cohesion among mammalian cancer cells. This aggregation is mediated by changes in the cell’s actin filaments, which are normally responsible for structural support and mobility. In multicellular organisms, actin filaments perform the additional function of cell-to-cell adhesion. This adhesion in multicellular organisms is what allows for the formation of tissues. However, cancer cells have an altered ability to perform such adhesions, which leads to metastasis, or the spreading of cancerous cells throughout the body. Metastasis is what differentiates fatal malignant cancers from benign tumors. Since D. discoideum is a single-celled organism, the ability of this organism to behave like a multicellular organism makes it ideal for research involving actin filaments. Also, the organism is easy to study due to its unicellular simplicity.  Scientific findings uncovered in Dictyostelium could provide a new way to regulate or limit the spread of cancer cells.

     Our research objective is to determine that, between two mutations in a protein kinase, TklA, and in the phospholipase, PldB,  which are known to cause de-adhesion, how are the genes ordered in terms of an upstream or downstream effect and which mutation would lead to a greater rate of de-adhesion. The mutation involving the protein kinase TklA is a deletion notated as tklA- and the mutation involving the phospholipase PldB is an overexpression notated as PldBoe. The double mutant, or a cell line with both the deletion of the protein kinase TklA gene and the overexpression of the phospholipase PldB, was a key component in identifying the order of these two transduction proteins in terms of which gene works downstream or upstream of the other. The way this would be determined is that if a gene were to act downstream of another upstream gene, the double mutant would have a similar phenotype to the downstream gene.


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Cancer Research